Efficacy and Mechanism of Preoperative Simvastatin Therapy on Myocardial Protection after Extracorporeal Circulation. (8th November 2017)

• Record Type: Journal Article
• Authors: Hua, Ping; Liu, Jianyang; Tao, Jun; Zou, Rongjun; Lin, Xifeng; Zhang, Dingwen; Yang, Songran
• Other Names: Aliev Gjumrakch Academic Editor.
• Is Part Of: BioMed research international. Volume 2017(2017)
• Publication Date: 2017-11-08
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2017/6082430
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Background . Cardiopulmonary bypass (CPB) causes systemic inflammatory response and ischemia-reperfusion (IR) injury. Objective . To investigate the effect and mechanism of simvastatin on myocardial injury in cardiac valve surgery with CPB. Methods . One hundred thirty patients were randomly assigned to the statin group (n = 65 ) or control group (n = 65 ). Simvastatin was administered preoperatively and postoperatively. Duration of intensive care unit stay, duration of assisted ventilation, and left ventricular ejection fraction were recorded. Plasma was analysed for troponin T (cTnT), isoenzyme of creatine kinase (CK-MB), tumor necrosis factor alpha (TNF-α ), interleukin-6 (IL-6), and interleukin-8 (IL-8). Ultrastructure of the myocardium and autophagosomes were observed. Beclin-1, LC3-II/I, P62, AMPK, and the phosphorylation of AMPK in cardiomyocytes were detected. Results . Simvastatin significantly reduced the duration of assisted ventilation (P = 0.030 ) and ejection fraction was significantly higher in the statin group (P = 0.024 ). Simvastatin significantly reduced the levels of cTnT, CK-MB, TNF-α, IL-6, and IL-8 (P < 0.05 ), reduced the expression of LC3-II/LC3-I and Beclin 1, and increased the expression of phosphorylation of AMPK. Simvastatin reduced the generation of autophagosomes and the ultrastructural injuries to myocardium. Conclusion . Perioperative statin therapy reduced myocardial injury by regulating myocardial autophagy and activating the phosphorylation of AMPK. The registration number of this study is ChiCTR-TRC-14005164 .